ISG56 is a negative-feedback regulator of virus-triggered signaling and cellular antiviral response

被引：174

作者：

Li, Ying ^{[1
]}

Li, Chao ^{[1
,2
]}

Xue, Peng

Zhong, Bo ^{[1
]}

Mao, Ai-Ping ^{[1
]}

Ran, Yong ^{[1
]}

Chen, He ^{[1
]}

Wang, Yan-Yi ^{[1
]}

Yang, Fuquan ^{[2
]}

Shu, Hong-Bing ^{[1
]}

机构：

[1] Wuhan Univ, Coll Life Sci, Wuhan 430072, Peoples R China

[2] Chinese Acad Sci, Inst Biophys, Beijing 100101, Peoples R China

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2009年 / 106卷 / 19期

基金：

中国国家自然科学基金;

关键词：

interferon; MITA; negative-feedback regulation; IRF3; NF-kappa B; NF-KAPPA-B; DOUBLE-STRANDED-RNA; RIG-I; ADAPTER PROTEIN; PATHOGEN RECOGNITION; INTERFERON; BETA; IDENTIFICATION; TRANSCRIPTION; ACTIVATION;

D O I：

10.1073/pnas.0900818106

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

IFN-stimulated gene 56 (ISG56) is one of the first identified proteins induced by viruses and type I IFNs. In this study, we identified ISG56 as a virus-induced protein associated with MITA, an adapter protein involved in virus-triggered induction of type I IFNs. Overexpression of ISG56 inhibited Sendai virus-triggered activation of IRF3, NF-kappa B, and the IFN-beta promoter, whereas knockdown of ISG56 had opposite effects. Consistently, overexpression of ISG56 reversed cytoplasmic poly(I:C)-induced inhibition of vesicular stomatitis virus (VSV) replication, whereas knockdown of ISG56 inhibited VSV replication. Competitive coimmunoprecipitation experiments indicated that ISG56 disrupted the interactions between MITA and VISA or TBK1, two components in the virus-triggered IFN signaling pathways. These results suggest that ISG56 is a mediator of negative-feedback regulation of virus-triggered induction of type I IFNs and cellular antiviral responses.

引用

页码：7945 / 7950

页数：6

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